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Abstract
Acute renal failure is commonly due to acute tubular necrosis (ATN), the latter representing
an acute, usually reversible loss of renal function incurred from ischemic or nephrotoxic
insults occurring singly or in combination. Such insults instigate a number of processes-hemodynamic
alterations, aberrant vascular responses, sublethal and lethal cell damage, inflammatory
responses, and nephron obstruction-that initiate and maintain ATN. Eventually, reparative
and regenerative processes facilitate the resolution of renal injury and the recovery
of renal function. Focusing mainly on ischemic ATN, this article reviews evidence
indicating that the inordinate or aberrant generation of reactive oxygen species (ROS)
may contribute to the initiation and maintenance of ATN. This review also discusses
the possibility that ROS may instigate adaptive as well as maladaptive responses in
the kidney with ATN, and raises the possibility that ROS may participate in the recovery
phase of ATN.